ArticleCell death & disease2018
Epigenetic inhibition of Wnt pathway suppresses osteogenic differentiation of BMSCs during osteoporosis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- The Effects of Sesquiterpene Lactones on the Differentiation of Human or Animal Cells CulturedFrontiers in pharmacology · 2022Pooled it
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Article
- Immunomodulatory-osteogenic dual-functional nanofibers augment screw anchorage in osteoporotic bone.Materials today. Bio · 2026Article
- The progress of m6A methylation-regulated non-coding RNAs in osteogenic differentiation and osteoporosis.Non-coding RNA research · 2026Review
- Bromodomain-Driven Regulation of Stem Cells: A Potential Target for Cancer Therapeutic Intervention.Stem cell reviews and reports · 2026Review
- Genetically reprogrammed BMSCs with Lamin B1 depletion enhance bone regeneration for osteoporosis therapy.Frontiers in bioengineering and biotechnology · 2026Article
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Multi-scale biomimetic fusion construction of cerium ion hydrogel-scaffold for promoting osteoporotic bone defect repair.Journal of orthopaedic translation · 2025Article
- Smart responsive biomaterials for spatiotemporal modulation of functional tissue repair.Materials today. Bio · 2025Review
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Augmenting osteoporotic osseointegration through a temporal release nanocoating-based reversing dysregulated osteogenic microenvironment.Journal of orthopaedic translation · 2025Article
- Unlocking the Epigenetic Symphony: Histone Acetylation Orchestration in Bone Remodeling and Diseases.Stem cell reviews and reports · 2025Review
- Identification of Programmed Cell Death-related Biomarkers for the Potential Diagnosis and Treatment of Osteoporosis.Endocrine, metabolic & immune disorders drug targets · 2025Article
- The canonical Wnt pathway in osteoporosis: a scoping review of key compounds and proteins modulating Wnt-induced osteogenesis.Frontiers in pharmacology · 2025Review
- Remote coupling of electrical and mechanical cues by diurnal photothermal irradiation synergistically promotes bone regeneration.Journal of nanobiotechnology · 2024Article
- Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease.Bone research · 2024Review
- Tumour necrosis factor α regulates the miR-27a-3p-Sfrp1 axis in a mouse model of osteoporosis.Experimental physiology · 2024Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disrupted Wnt signaling in osteoblastic-lineage cells leads to bone formation defect in osteoporosis. However, the factors repressing Wnt signaling are unclear. In our study, we found that Wnt signaling was suppressed persistently in bone marrow-derived mesenchymal stem cells (BMSCs) during osteoporosis. Accordingly, histone acetylation levels on Wnt genes (Wnt1, Wnt6, Wnt10a, and Wnt10b) were declined in BMSCs from OVX mice. By screening the family of histone acetyltransferase, we identified that GCN5 expression increased during osteogenic differentiation of BMSCs, whereas decreased after osteoporosis. Further analysis revealed that GCN5 promoted osteogenic differentiation of BMSCs by increasing acetylation on histone 3 lysine 9 loci on the promoters of Wnt genes. Reduced GCN5 expression suppressed Wnt signaling, resulting in osteogenic defect of BMSCs from OVX mice. Moreover, restoring GCN5 levels recovered BMSC osteogenic differentiation, and attenuated bone loss in OVX mice. Taken together, our study demonstrated that disrupted histone acetylation modification in BMSCs lead to bone formation defect during osteoporosis. The findings also introduced a novel therapeutic target for osteoporosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.